With increasing age, the risk of developing chronic health conditions also increases, and many older people suffer from multiple co-existing health conditions, i.e., multimorbidity. One common health condition at older age is hearing loss (HL). The current article reflects on the implications for audiological care, when HL is one of several health conditions in a multimorbidity. An overview of health conditions often co-existing with HL, so called comorbidities, is provided, including indications for the strength of the associations. The overview is based on a literature study examining cohort studies that were published in the years 2010-2018 and examined associations of hearing loss with other health conditions, namely Visual impairment, Mobility restrictions, Cognitive impairment, Psychosocial health problems, Diabetes, Cardiovascular diseases, Stroke, Arthritis, and Cancer. This selection was based on previous publications on common chronic health conditions at older age and comorbidities of hearing loss. For all of these health conditions, it was found that prevalence is larger in people with a HL and several longitudinal studies also found increased incident rates in people with a HL. The examined publications provide little information on how hearing loss should be managed in the clinical care of its comorbidities and vice versa. The current article discusses several options for adaptations of current care. Nonetheless, solutions for an integrated audiology care model targeting HL in a multimorbidity are still lacking and should be subject to future research.

An intricate interplay between circadian and sleep-wake homeostatic processes regulate cognitive performance on specific tasks, and individual differences in circadian preference and sleep pressure may contribute to individual differences in distinct neurocognitive functions. Attentional performance appears to be particularly sensitive to time of day modulations and the effects of sleep deprivation. Consistent with the notion that the neuromodulator, adenosine adenosine , plays an important role in regulating sleep pressure, pharmacologic and genetic data in animals and humans demonstrate that differences in adenosinergic tone affect sleepiness, arousal and vigilant attention attention in rested and sleep-deprived states. Caffeine Caffeine -the most often consumed stimulant in the world-blocks adenosine receptors and normally attenuates the consequences of sleep deprivation on arousal, vigilance, and attention. Nevertheless, caffeine cannot substitute for sleep, and is virtually ineffective in mitigating the impact of severe sleep loss on higher-order cognitive functions. Thus, the available evidence suggests that adenosinergic mechanisms, in particular adenosine A2A receptor-mediated signal transduction, contribute to waking-induced impairments of attentional processes, whereas additional mechanisms must be involved in higher-order cognitive consequences of sleep deprivation. Future investigations should further clarify the exact types of cognitive processes affected by inappropriate sleep. This research will aid in the quest to better understand the role of different brain systems (e.g., adenosine and adenosine receptors) in regulating sleep, and sleep-related subjective state, and cognitive processes. Furthermore, it will provide more detail on the underlying mechanisms of the detrimental effects of extended wakefulness, as well as lead to the development of effective, evidence-based countermeasures against the health consequences of circadian misalignment and chronic sleep restriction. In press (accepted): January 14, 2014 Addresses for correspondence:Hans-Peter Landolt, Ph.D.

BackgroundCoffee consumption is a known inducer of cytochrome P450 1A2 (CYP1A2) enzyme activity. We recently observed that a group of type-2 diabetes patients consumed more caffeine (coffee) on a daily basis than non-type-2 diabetes controls. Here, we investigated whether type-2 diabetes cases may metabolize caffeine faster than non-type-2 diabetes controls.MethodsTo estimate CYP1A2 enzyme activity, an established marker of caffeine metabolism, we quantified the paraxanthine/caffeine concentration ratio in saliva in 57 type-2 diabetes and 146 non-type-2 diabetes participants in a case–control field study. All participants completed validated questionnaires regarding demographic status, health and habitual caffeine intake, and were genotyped for the functional -163C > A polymorphism of the CYP1A2 gene.ResultsIn the diabetes group, we found a larger proportion of participants with the highly inducible CYP1A2 genotype. Furthermore, the paraxanthine/caffeine ratio, time-corrected to mitigate the impact of different saliva sampling times with respect to the last caffeine intake, was higher than in the control group. Participants who reported habitually consuming more caffeine than the population average showed higher CYP1A2 activity than participants with lower than average caffeine consumption. Multiple regression analyses revealed that higher caffeine intake was potentially an important mediator of higher CYP1A2 activity.ConclusionsEstimated CYP1A2 enzyme activity, and thus speed of caffeine metabolism, was higher in our type-2 diabetes group; this was possibly due to higher intake of caffeine, a known inducer of CYP1A2 enzyme activity. Given the fairly small sample sizes, the results need to be considered as preliminary and require validation in larger populations.Electronic supplementary materialThe online version of this article (doi:10.1186/s12986-016-0126-6) contains supplementary material, which is available to authorized users.

Type 2 diabetic patients may self-medicate with caffeine to alleviate daytime sleepiness. High caffeine intake reflects a lifestyle factor that may be considered when promoting type 2 diabetes management.